INT142678

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Context Info
Confidence 0.51
First Reported 2007
Last Reported 2009
Negated 0
Speculated 0
Reported most in Abstract
Documents 4
Total Number 5
Disease Relevance 2.10
Pain Relevance 1.60

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

cytosol (Mapk9) mitochondrion (Mapk9) nucleus (Mapk9)
kinase activity (Mapk9) transcription factor binding (Mapk9) cytoplasm (Mapk9)
Anatomy Link Frequency
PSC 2
Mapk9 (Mus musculus)
Pain Link Frequency Relevance Heat
Paracetamol 12 99.82 Very High Very High Very High
Leflunomide 10 99.52 Very High Very High Very High
cINOD 2 91.64 High High
Nerve growth factor 2 62.00 Quite High
Analgesic 1 58.08 Quite High
fibrosis 6 50.00 Quite Low
Chronic pancreatitis 2 5.00 Very Low Very Low Very Low
Inflammation 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Apoptosis 6 100.00 Very High Very High Very High
Colon Cancer 8 96.96 Very High Very High Very High
Death 3 96.96 Very High Very High Very High
INFLAMMATION 4 91.44 High High
Hepatotoxicity 4 88.00 High High
Injury 2 75.00 Quite High
Toxicity 1 66.60 Quite High
Fibrosis 6 60.20 Quite High
Pancreatitis 2 5.00 Very Low Very Low Very Low
Cancer 2 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
DIM-C-pPhOCH(3) also activated the extrinsic apoptosis pathway through increased phosphorylation of c-jun N-terminal kinase which, in turn, activated C/EBP homologous transcription factor (CHOP) and death receptor 5 (DR5).
Positive_regulation (increased) of Phosphorylation (phosphorylation) of c-jun N-terminal kinase associated with apoptosis and death
1) Confidence 0.51 Published 2008 Journal Mol. Carcinog. Section Abstract Doc Link 17957723 Disease Relevance 0.76 Pain Relevance 0.12
DIM-C-pPhOCH(3) also activated the extrinsic apoptosis pathway through increased phosphorylation of c-jun N-terminal kinase which, in turn, activated C/EBP homologous transcription factor (CHOP) and death receptor 5 (DR5).
Positive_regulation (activated) of Phosphorylation (phosphorylation) of c-jun N-terminal kinase associated with apoptosis and death
2) Confidence 0.37 Published 2008 Journal Mol. Carcinog. Section Abstract Doc Link 17957723 Disease Relevance 0.78 Pain Relevance 0.12
Halofuginone increased c-Jun N-terminal kinase phosphorylation in PSCs derived from cerulein-treated mice.
Positive_regulation (increased) of Phosphorylation (phosphorylation) of c-Jun N-terminal kinase
3) Confidence 0.35 Published 2009 Journal Pancreas Section Body Doc Link 19188864 Disease Relevance 0.06 Pain Relevance 0
CONCLUSIONS: Halofuginone inhibits Smad3 phosphorylation and increases c-Jun N-terminal kinase phosphorylation, leading to the inhibition of PSC activation and consequent prevention of fibrosis.
Positive_regulation (increases) of Phosphorylation (phosphorylation) of c-Jun N-terminal kinase in PSC
4) Confidence 0.35 Published 2009 Journal Pancreas Section Body Doc Link 19188864 Disease Relevance 0 Pain Relevance 0
Instead, leflunomide inhibited APAP-induced activation (phosphorylation) of c-jun NH2-terminal protein kinase (JNK), thus preventing downstream Bcl-2 and Bcl-XL inactivation and protecting from mitochondrial permeabilization and cytochrome c release.
Positive_regulation (activation) of Phosphorylation (phosphorylation) of c-jun NH2-terminal protein kinase associated with paracetamol and leflunomide
5) Confidence 0.18 Published 2007 Journal Hepatology Section Abstract Doc Link 17366662 Disease Relevance 0.50 Pain Relevance 1.36

General Comments

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